Author

G. Stary

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Immunology· 3

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:drug response / drug discovery· 2 Research Focus:host-pathogen & immune response· 2 Organism:human· 2 Assay:proteomics· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

A. Haschemi· 1 shared A. P. Kutschat· 1 shared A. Redl· 1 shared B. Homey· 1 shared B. L. Turnes· 1 shared C. Freystaetter· 1 shared C. J. Woolf· 1 shared D. Krauss· 1 shared

Activity by Year

2023-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 17 mutual co-author links

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1 shared paperImmunology

A. Haschemi

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Spermidine/spermine N1-acetyltransferase controls tissue-specific regulatory T cell function in chronic inflammation

T. Neuwirth, D. Malzl, K. Knapp, P. Tsokkou, L. Kleissl, A. Redl, C. Freystaetter, N. Marella, A. P. Kutschat, E. Ponweiser, A. Haschemi, D. Seruggia, J. Menche, E. F. Wagner, G. Stary

The paper identifies SAT1 as a marker of skin-specific Treg dysfunction in TH17-mediated inflammation and shows targeting SSAT can rescue Treg function in a mouse model.

bioRxiv · Mar 25, 2024 · PreprintImmunology

Scarring hair follicle destruction is driven by the collapse of EGFR-protected JAK-STAT1-sensitive stem cell immune privilege

K. Strobl, J. Klufa, R. Jin, L. Artner-Gent, D. Krauss, P. Novoszel, J. Strobl, G. Stary, I. Vujic, J. Griss, M. Holcmann, M. Farlik, B. Homey, M. Sibilia, T. Bauer

This study shows that EGFR protects hair follicle stem cells from immune-mediated damage by maintaining JAK-STAT1-sensitive immune privilege, and its disruption leads to scarring hair loss, which can be reversed by JAK1/2 inhibition.

bioRxiv · Oct 11, 2023Immunology

Mast cell-derived BH4 is a critical mediator of postoperative pain

P. Starkl, G. Jonsson, T. J. Artner, B. L. Turnes, N. Serhan, T. Oliveira, L.-M. Gail, K. Stejskal, K. Channon, T. Kocher, G. Stary, V. Klang, N. Gaudenzio, S. Knapp, C. J. Woolf, , S. J. F. Cronin

This study identifies mast cell-derived BH4 as a key mediator of postoperative pain, showing that substance P triggers BH4-dependent serotonin release in mast cells, and blocking substance P reduces pain.

bioRxiv · Jan 24, 2023 · PreprintImmunology